Interleukin‐2, Interleukin‐7, T cell‐mediated autoimmunity, and N‐glycosylation

T cell activation and self‐tolerance are tightly regulated to provide effective host defense against foreign pathogens while deflecting inappropriate autoimmune responses. Golgi Asn (N)‐linked protein glycosylation coregulates homeostatic set points for T cell growth, differentiation, and self‐tolerance to influence risk of autoimmune disorders such as multiple sclerosis (MS). Human autoimmunity is a complex trait that develops from intricate and poorly understood interactions between an individual's genetics and their environmental exposures. Recent evidence from our group suggests that in MS, additive and/or epistatic interactions between multiple genetic and environmental risk factors combine to dysregulate a common biochemical pathway, namely Golgi N‐glycosylation. Here, we review the multiple regulatory mechanisms controlling N ‐glycan branching in T cells and autoimmunity, focusing on recent data implicating a critical role for interleukin‐2 (IL‐2) and IL‐7 signaling.